Significance The precise roles of E-cadherin in the liver and liver carcinogenesis are still unknown. Here we show that mice lacking E-cadherin in the liver develop spontaneous periportal inflammation via an impaired intrahepatic biliary network, as well as periductal fibrosis, which resembles primary sclerosing cholangitis. Inducible gene knockout studies identified E-cadherin loss in biliary epithelial cells as a causal factor of cholangitis induction, and dysregulated E-cadherin expression was also seen in patients with primary sclerosing cholangitis. E-cadherin loss also significantly accelerates genetically and chemically engineered liver cancer through epithelial–mesenchymal transition, up-regulation of stem cell markers, and ERK activation. Thus, E-cadherin plays critical roles in maintaining homeostasis and suppressing carcinogenesis in the liver.

No abstract

By oligonucleotide-directed mutageneses, 13 substitutions of amino acids at the carboxy-terminal region of rat liver cytochrome P-450d were done as follows: (A) Phe-449----Tyr; (B) Gly-450----Ser; (C) Leu-451----Ser; (D) Gly-452----Glu; (E) Lys-453----Glu; (F) Arg-454----Leu; (G) Arg-455----Gly; (H) Cys-456----Tyr; (I) Cys-456----His; (J) Ile-457----Ser; (K) Gly-458----Glu; (L) Glu-459----Ala; (M) Ile-460----Ser. The CO-bound reduced forms of the wild type and mutants B-G, J, L, and M gave Soret peaks at 448 nm. The CO complex of mutant A gave a Soret peak at 445 nm. The intensities of the CO-bound forms of mutants A, C, D, and J were very small compared with that of the wild-type complex. The CO-reduced forms of mutants H, I, and K did not give a Soret peak around 450 nm at all. The 448-nm peak of mutant F was unstable and quickly disappeared with the concomitant appearance of a peak at 420 nm.(ABSTRACT TRUNCATED AT 250 WORDS)

Biliary interventions via DBE using a short enteroscope are feasible in patients with surgical anatomy.

We observed broadband emission spectra of Cs-He excimers (Cs*He) in cold He gas (1.3-100 K), when Cs atoms were excited to the 6 2 P states. We calculated the emission spectrum from each vibrational state of Cs*He using Pascale's semiempirical Cs-He potential energy curves ͓J. Pascale, Phys. Rev. A 28, 632 ͑1983͔͒, and compared the results with the observed spectra. From the measured spectral shape, we estimated the relative populations of the vibrational states of Cs*He at various He gas densities, and estimated the predissociation rate of Cs*He in the A 2 ⌸ 1/2 state. Moreover, a broadband emission spectrum of Cs*He 2 was also observed, which was compared with that observed in liquid He.